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01. Step 1 mine > Immunology > Flashcards

Immunology Flashcards

1
Q

Natural Killer (NK) cells are responsible for killing:

A

Virus infected or Tumor cells

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2
Q

Virus-infected or tumor cells need to have _______ to be killed by NK cells

A

Decreased or absent MHC class I protein

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3
Q

Do NK cells naturally lyse cells?

A

No. They have perforins and granzymes.

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4
Q

Immunoglobulin g (IgG) and Complement C3b are examples of:

A

Opsonins. They work in similar manners to allow phagocytes to phagocyte foreign cells.

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5
Q

Where is the site of COMPLEMENT binding in the immunoglobulin molecule shown below?

A

D. In the Fc portion closer to the hinge region

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6
Q

Which antibodies can trigger the classical complement pathway?

A

IgG and IgM

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7
Q

Major immune mechanisms against Giardia Lamblia (parasites)

A

CD4+ Th cells and secretory IgA production (impairs adherence to bowel mucosa)

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8
Q

Children with these diseases have a predisposition for chronic Giardiasis (parasite)

A

IgA Deficiency

X-linked aggamaglobulinemia

Common variable immune deficiency

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9
Q

+ Positive selection is responsible for:
And occurs in:

A

Positive selection: only T cells expressing a TCR able to bind self MHC are able to survive.

Thymic cortex.

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10
Q

- Negative selection is the process for:

Occurs in:

A

T cells with TCR that binds with very high affinity to cell antigen or MHC class I or II are eliminated (apoptosis)

Negative selecion occurs in thymic medulla

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11
Q

Process that eliminates T cells that are overly autoreactive against cell antigens.
May cause autoimmunity if not destroyed.

A

Negative selection. (Eliminates T cells that bind self MHC or self antigens with overly high affinity)

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12
Q

___________ prevent the hematogenous spread of candida (prevents disseminated candidiasis)

A

Neutrophils.
*Neutropenic or immunocompromised patients may have candidiasis in blood

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13
Q

Patients with HIV (low T-cell count) have increased risk of ___________ candidiasis

A

Superficial.

(oral/esophageal, cutaneous, vulvovaginitis)

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14
Q

Programmed Death receptor (PD-1) is expressed on the surface of _________

A

Activated T cells.

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15
Q

When PD-1 (on activated T cells) bind to their PD-L1 ligand:

A

Inhibit cytotoxic T cells

(Downregulate immune response, help tumor cells survive)

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16
Q

CD28 on T cell binds to _____ on _____ to activate T cell

A

B7 on APC

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17
Q

Chronic Granulomatous Disease is caused by a defect in:

A

NADPH oxidase

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18
Q

Clinical manifestations of Chronic Granulomatous Disease

A
  • Recurrent Catalase + infections (bact+fungi)
  • Diffuse granuloma formation
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19
Q

NADPH oxidase catalizes the reduction of O2 to ______
This occurs in this structure:_________

A

O2- (superoxide)

Phagolysosomes

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20
Q

Absence of green fluorescence on dihydrorhodamine test:

A

Lack of NADPH oxidase = Chronic Granulomatous Disease

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21
Q

Nitroblue Tetrazolium (NTB) test detects:

A

NADPH oxidase defect in Chronic Granulomatous Disease.

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22
Q

Th1 cyokine that is a key factor in elimination of micobacterium infections

A

IFN - gamma

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23
Q

Macrophages infected with mycobacterium produce _____ which in turn, stimulates T cells and NK cells to produce ____

A

IL-12 (macrophages)

IFN-gamma (T cells and NK)

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24
Q

Inherited defects involving the IFN-gamma signaling pathway result in

A

Disseminated mycobacterial disease in infancy

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25
Q

Clinical presentation of Primary Ciliary Diskinesia

(Kartagener Sx) - AutRes

A

- Chronic sinusitis

- Bronchiectasis

- Dextrocardia / Situs inversus

  • Infertility
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26
Q

Failure of Dynein arms in cilia to develop normally

A

Primary Cilliary Diskinesia or Kartagener Syndrome

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27
Q

Implicated maternal antibodies in erythroblastosis fetalis and hemolytic disease of the newborn

A

IgG (only Ig that crosses the placenta)

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28
Q

If a mother is blood type B and the baby is A, the maternal antibodies formed are:_____

Risk of erythroblastosis fetalis? _____

A

Anti-A (IgM)

No risk. IgM does NOT cross the placenta

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29
Q

If a mother is blood type O and the baby is B, the maternal antibodies formed are____

Risk of erythroblastosis fetalis?_____

A

Anti-B and anti-A

Yes. IgG cross the placenta.

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30
Q

Can Rh disease occur in the FIRST pregnancy?

A

No.

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31
Q

Can ABO disease occur in the FIRST pregnancy?

A

Yes

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32
Q

Region of the lymph node populated by T lymphocytes and dendritic cells.

Affected in DiGeorge syndrome (22q.11)

A

Paracortex

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33
Q

Antigen present in blood of Rh + individuals

A

D antigen

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34
Q

Risk of transplacental fetomaternal blood exchange increases with_______ and is highest during ________

A

Increasing gestational age

Highest during delivery

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35
Q

Anti-Rh(D) immune globulin (IgG anti-D) is administered to Rh neg women at _____ weeks and _____

A

28 weeks gestation and

immediate postpartum period

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36
Q

Seronegative spondyloarthropathies (4)

A
  • Ankylosing spondylitis
  • Reactive arthritis
  • Arthritis associated with IBD
  • Psoriatic arthritis
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37
Q

Specific Human Leukocyte Type I (HLA I) serotype associated with Ankylosing Spondylitis

A

HLA-B27

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38
Q

Class I HLA proteins, localization and function

A

HLA-A, HLA-B, HLA-C

Present in ALL nucleated cells

Present endogenous antigens to CD8+ cytotoxic T cells.

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39
Q

HLA Class II proteins, location and function

A

HLA-DP, HLA-DQ, HLA-DR

Present in APCs (macrophages, dendritic cells)

Present FOREIGN antigens to CD4+ helper cells.

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40
Q

Finding

A

Fusion of sacroiliac joints seen in:

Ankylosing Spondylitis (HLA-B27) MHC Class I

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41
Q

Is there a positive or negative serum rheumatoid factor in this 27 year old man with morning stiffness and low back pain?

A

Sclerosis, ligamentous calcification and vertebral fusion = Ankylosing Spondylitis (one of the seroNEGATIVE spondyloarthropaties) so serum Rheumatoid Factor is NEGATIVE. but HLA-27 +

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42
Q

Hyperacute rejection occurs in minutes to hours and is secondary to:

A

Preformed antibodies against graft in recipient’s circulation.

(Fibrinoid necrosis and capillary thrombotic occlusion, mottling and cyanosis)

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43
Q

Acute rejection occurs in _______ (time)

A

< 6 months

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44
Q

Exposure to DONOR antigens induces humoral/cellular activation of naive immune cells in this type of rejection

A

Acute rejection (< 6 months)

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45
Q

In this type of transplant rejection, there is:

  • Vascular wall thickening & luminal narrowing
  • Interstitial fibrosis & parenchyma atrophy
A

Chronic rejection (months to years, low-grade immune response, refractory to immunosuppresants)

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46
Q

Chronic renal allograft rejection presents with:

A
  • Worsening hypertension
  • Slowly progessive rise in serum creatinine
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47
Q

Structure of MHC class I protein

A

Single heavy chain + ß2-microglobulin

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48
Q

Presents antigen to CD8+ cytotoxic T-cells

A

MHC class I

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49
Q

Type of antigen presented to CD8+ T-cells by MHC class I proteins

A

Viruses

Tumor proteins

(Antigens processed in cytoplasm)

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50
Q

MHC class II proteins present antigen to______

A

CD4+ helper T-cells

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51
Q

Type of antigen presented to CD4+ helper lymphocytes by MHC class II

A

Bacterial

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52
Q

Antigen presentation in MHC class II (to CD4+) results in:

A
  • Activation of Th cells
  • Stimulation of humoral and cell-mediated immune response
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53
Q

Anaphylaxis is a systemic type ____ hypersensibility reaction

A

1

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54
Q

Anaphylaxis is secondary to:

  • ________ & _________ degranulation and resultant ________ & ________ release
A
  • Mast cell & basophil degranulation

- Hystamine & Tryptase release

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55
Q

Elevated serum levels of _______ are used to support clinical diagnosis of Anaphylaxis

A

Tryptase (released by mast cells)

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56
Q

The high-affinity IgE receptor is found on ________ & _________ and plays a primary role in mediating the allergic response

A

mast cells & basophils

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57
Q

Aggregation of the high-affinity IgE receptor on the mast cell surface leads to:

A

Mast cell and basophil degranulation + release of hystamine and tryptase = allergic response (Anaphylaxis)

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58
Q

When a graft becomes cyanotic and mottled immediately after blood vessels connected to those of recipient, there is a ____________ mediated hypersensitivity

A

Antibody mediated hypersensitivity

(Hyperacute rejection –> Preformed ANTIBODIES against graft, already in patient’s circulation)

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59
Q

Hyperacute rejection is an antibody-mediated reaction (Type ____ hypersensitivity reaction)

Caused by preformed ______ antibodies.

A
  • Type II hypersensitivity reaction
  • IgG
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60
Q

Small allergenic substance responsible for immune response in poison ivy dermatitis:

________________

Associated with _____ cells

A

Uroshiol

CD8+ T-cells (keratinocyte apoptosis)

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61
Q

Contact dermatitis is a Type ______ hypersensitivity reaction

A

Type IV hypersensitivity reaction

(delayed-type)

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62
Q

In Type IV hypersensitivity reaction, there are 2 phases:

  1. ___________ (and duration)
  2. ____________ (and duration)
A
  1. Sensitization phase (10 - 14 days)
  2. Elicitation phase (2 - 3 days)
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63
Q

In this phase of type IV hypersensitivity, hapten-specific T cells are created.

A

Phase 1. Sensitization (Cutaneous dendritic cells - Langerhans - take haptens and express them in MHC-I and II)

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64
Q

Exposed skin in a wood worker or someone near wood that develops an erythematous linear rash with excoriation should make us think in:

A

Uroshiol - induced type IV hypersensitivity

(CD8+ T-cells - keratynocyte apoptosis)

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65
Q

Patient with T cell function intact but complete absence of mature B cells + severe deficiency of ALL immunoglobulin types:

A

X-linked agammaglobulinemia (Bruton)

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66
Q

In a patient with intact T-cell function but lack of mature B-cells and complete lack of all immunoglobulins, which structure is lacking in their lymph nodes?

A

Germinal centers (Where B-cells mature)

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67
Q
A
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68
Q

If an asymptomatic patient is:

IgM negative for Hep A &

IgG positive for Hep A

but has NOT received vaccine, what is the cause of his laboratories?

A

He probably had anicteric Hep A when he was a toddler.

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69
Q

Hepatitis A virus infection is most commonly silent or subclinical (anicteric) in: ______ ________

A

Young children

(< 6 years, 80% asymptomatic)

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70
Q

HBsAg first appears ________ (before, after) onset of symptoms, peak when the patient is most ill and becomes undetectable in ________ months

A

HBsAg appears before onset of Hep B symptoms

Normally, HBsAg becomes undetectable in 3-6 months

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71
Q

HBeAg and HBV DNA detected in serum are markers of:

A

Active Hep B virus replication

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72
Q

If HBsAg continues to be detectable after 6 months, the patient now has:

A

Chronic Hep B

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73
Q

If there is a persistence of HBeAg +

lack of anti-HBeAg, the patient most probably has:

A

Highly infectious chronic B Hepatitis

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74
Q

In Hep B, once the acute disease has resolved, _________ Ig____ arises.

This antibody confers lifelong immunity.

A

Anti-HBsAg IgG

*Remember: if HBsAg persists more than 6 months: it’s chronic.

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75
Q

If a pediatric patient arrives with dysphagia, breathing difficulty (inspiratory stridor), drooling and a cherry red epiglottis, you think of: __________ that is caused by: _____________

A

Acute Epiglottitis

Caused by Haemophilus influenzae type b in children

(Hib vaccine REQUIRED, if a child has epiglottitis you think his parents are some piece of shit antivaxxers or the kid is vaccined but has BAD luck!)

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76
Q

Surface marker of macrophages

A

CD-14

(Macrofourteenphages™)

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77
Q

The caseating granulomas in tuberculosis consist on large epithelial _________ with _____ _____ granular cytoplasm surrounding a central region of necrotic debris.

A

Macrophages

Pale pink cytoplasm

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78
Q

Child with
- Severe bacterial and viral infections in infancy

  • Chronic diarrhea
  • Mucocutaneous candidiasis

Dx?

A

Severe Combined Immunodeficiency (SCID)

Severe bacterial and viral infections

Candidiasis (mucocutaneous)

Immunocompromised

Diarrhea (chronic)

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79
Q

Very low or absent CD3+ T cells

and

Very low gamma globulin levels

Dx?

A

SCID (Severe Combined Immune Deficiency)

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80
Q

Thymic hipoplasia or aplasia seen in:

A

- DiGeorge syndrome (failure in formation of 3rd and 4th branquial pouches)

- SCID (Severe Combined Immune Deficiency) b/c of severe T cell deficiency

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81
Q

In a child with oculocutaneous albinism, pyogenic infections and progressive neurologic disfunction, you think about: ______________

That is caused by: _____________

A

Chediak-Higashi syndrome

Caused by impairment in microtubule function + failure in phagolysosome formation

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82
Q

In a child with conotruncal cardiac abnormalities, hypocalcemia and craniofacial abnormalities, you think about:

A

DiGeorge syndrome (22q.11)

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83
Q

Triad of:

  1. Recurrent infections that worsen with age (viral, bacterial and fungal)
  2. Easy bleeding (thrombocytopenia)
  3. Eczema

you think about:

A

Wiskott-Aldrich syndrome

(Abnormal functioning of cytoskeleton in cells + no function in B and T cells)

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84
Q

Immunodeficiency syndrome caused by insufficient production of mature B cells.

(Predisposition to infection by encapsulated pyogenic bacteria)

A

X-linked agammaglobulinemmia (Bruton)

En Bruton estás bien Bruto (no maduras) y te faltan celulas B maduras

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85
Q

Form of dendritic cell most commonly found in the skin

A

Langerhans cell (tennis raquet)

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86
Q

This APC expresses both MHC class II and

co-stimulatory B7 surface molecules

A

Dendritic cells.

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87
Q

Plays a role in granulomatous inflammation

(B. Langerhans cell)

(A. Langhans cell)

A

Langhans

(multinucleated giant cell, horseshoe arrangement, multiple nuclei)

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88
Q

Which Streptococcus pneumoniae vaccine is recommended in older adults >65 years but NOT in children < 2 years?

(Polysaccharidae vs. conjugate)

A

Polysaccharidae strep pneumo vaccine for old folks.

Protects against a wider range of serotypes but it is not immunogenic in children younger than 2 years (immature humoral response)

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89
Q

This vaccine contains a nontoxic diphteria protein conjugated to polysaccharides, recruits T cells, develops memory B cells and lowers mucosal carriage (herd immunity)

Name and what is it against?

A

13-valent pneumococcal conjugate vaccine against Streptococcus pneumoniae

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90
Q

Examples of live-attenuated vaccines

A

- Rotavirus

- Varicella

- Measles-Mumps-Rubella (MMR)

  • Adenovirus
  • Polio (Sabin)
  • Smallpox
  • BCG
  • Influenza (intranasal)
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91
Q

Autosomal Recessive syndrome consisting of:

  • Immunodeficiency
  • Albinism
  • Neurologic defects (nystagmus, peripheral and cranial neuropathies)
A

Chediak - Higashi

(Defect in neutrophil phagosome-lysosome fusion) = abnormal giant lysosomal inclusions

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92
Q

What type of hypersensitivity reaction presents immediately?

A

Type I (Anaphylaxis and Allergies)

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93
Q

Type of hypersensitivity reactions that activate Complement

A

Type II (cytotoxic) and Type III (immune complex)

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94
Q

Humoral and cellular components of type I hypersensitivity

A

Basophils & Mast cells

IgE

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95
Q

PostStreptococcal Glomerulonephritis (strep pyogenes) is a type _____ hypersensitivity reaction

A

PSGN is type III

(immune complex - deposition of antibody-antigen complexes)

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96
Q

Type I hypersensitivity reactions are mediated by the interaction of _______ with preexisting Ig___ bound to _______ & ________

A

Allergen (antigen)

IgE

Basophils & Mast cells

(+ cross-linking and degranulation)

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97
Q

High-affinity IgE receptor activation occurs by:

A

Aggregation of IgE receptor

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98
Q

Deficient communication between T CD4+ activated cells and B lymphocytes with:

  • Deficient CD40L-CD40 interaction
  • Failure of antibody class switching in B cells
A

Hyperimmunoglobuin M syndrome (Hyper IgM)

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99
Q

Child with:

  • Recurrent sinopulmonary & gastrointestinal infection
  • Infections with opportunistic pathogens (Pneumocystis, Criptosporidium)
  • Failure to thrive
  • LOW IgG, IgE and IgA
A

Hyperimmunoglobulin M syndrome (HyperIgM)

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100
Q

In B cells, during class switching to produce different immunoglobulins, which chain stays the same? Which chain undergoes DNA splicing until desired isotype is reached?

A
  • Variable region (antigenic specificity of antibody) stays the same
  • Heavy chain constant region undergoes DNA splicing
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101
Q

Class switching of immunoglobulins occurs when CD___+ T cell is activated and uses its CD____ ligand to bind to CD____ on B cell surface.

A

CD4+ T cells activated

Use CD40L (ligand)

binds to CD40 on B cells

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102
Q

In HyperIgM syndrome, the most common cause is:

a) Lack of CD40 on B cells
b) Lack of CD40L on T cells

And it is inherited in a __________ pattern

A

b) Lack of CD40 LIGAND is most common

HyperIgM is inherited in a X-linked recessive pattern

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103
Q

Hilar adenopathy, pulmonary infiltrates and non-caseating lung granulomas in an African American female

A

Sarcoidosis!

*Non-caseating granulomas are sarcoidosis until proven otherwise.

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104
Q

Sarcoidosis is a _____ - mediated immune response to an unidentified antigen that results in the formation of ____________

A

Cell-mediated

granulomas

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105
Q

Cell-mediated immunity is driven by:

CD__+ , Th____ cells that secrete

IL-____ and ___-___

A

Cell-mediated immunity:

CD4+ Th1**

secrete IL-_2_ and IFN-gamma

106
Q

In cell-mediated immunity CD4+ Th1 cells secrete IL-2, which function is to:

A

Stimulate AUTOcrine proliferation of Th1 cells

107
Q

In cell-mediated immunity, the formation of granulomas is promoted by ____-____ which is secreted by __________ which in turn, were activated by _________

A

Formation of granulomas is promoted by IFN-gamma which is secreted by macrophages which were activated by IL-2 (which was secreted by CD4+ Th1 cells

108
Q

Humoral response is driven by Th____ CD__+ cells.

A

Th2, **CD4+** cells drive humoral response.

(You need two to humor)

109
Q

The products of Th2 CD4+ cells include:

IL-___ which promotes IgE antibody production by B cells &

IL-___ which promotes the production and activation of eosinophils and B-cell synthesis of IgA

A

IL-_4_ = IgE ab production in B-cells

IL-_5_ = eosinophil production&activation and IgA

110
Q

Deficiency of the complement factors that form the membrane attack complex result in recurrent infections by ___________ species

A

Neisseria

(i.e. bacterial meningitis caused by N. meningitidis in a college dorm)

111
Q

Complement factors that form the MAC (Membrane Attack Complex) and fuction

A

C5b, C6, C7, C8, C9

(C5b-C9)

MAC forms a pore in BACTERIAL cell membrane, leading to electolyte disturbances

112
Q

Binding of Type I interferons (alpha and beta) on infected and neighbouring cells results in:

A

Transcription of antiviral enzymes that HALT PROTEIN SYNTHESIS

113
Q

Antiviral enzyme transcription and halting of protein synthesis secondary to IFN alpha and beta becomes active ONLY in the presence of:

A

Double-stranded RNA

(which forms in infected cells that have viral replication) = selective protein synthesis inhibition - only in infected cells.

114
Q

Starting at age 2 months, children should receive which kind of vaccine vs Haemophilus influenzae serotype b? Why?

A

The Hib polysaccharidae-protein CONJUGATE vaccine because it elicits both a T-cell dependent immune response as well as an antibody mediated (B-cell) immune response.

115
Q

Haemophilus influenzae type B is an encapsulated gram-neg cocobacillus.

Which part of this bacteria is responsible for causing an antibody-mediated (B-cell) immune response?

A

The polysaccharidae capsule

- primary antigenic constitutent of vaccines for encapsulated bacteria

(Hib, Strep pneumo and N. meningitidis are all encapsulated and antiphagocitic)

116
Q

How does the Hib conjugate vaccine increase immunogenicity ?

A

With a carrier protein

(derived from TT-tetanus toxoid or Outer Membrane Protein OMP from N. meningitidis)

Carrier protein induces a T-cell dependent stimulation of B-lymphocytes = production of memory B-lymphocytes.

117
Q

Inactivated versions of the influenza vaccine function mainly by neutralizing antibodies against the ___________ antigen

A

Neutralizing antibodies against the

Hemagglutinin antigen

(inhibit binding of hemagglutinin to sialylated receptors on host cell membrane)

118
Q

When a patient is vaccinated vs influenza and later develops natural infection, does the virus infect the host cell?

A

No.

Neutralizing antibodies inhibit binding of hemagglutinin to sialylated receptors on host cell membrane and prevents the live virus from entering cells via endocytosis.

119
Q

Calcineurin is an essential protein in activation of IL-____ which promotes the growth and differentiation of ____-cells

A

Calcineurin activates IL-2

IL-2 promotes growth and differentiation
of T-cells

120
Q

Cyclosporine and tacrolimus are immunosupressants used in transplant patients and they act by inhibiting ________ which in turn, activates IL-____

A

Cyclosporine and tacrolimus inhibit CALCINEURIN activation (which in turn inhibits IL-2)

121
Q

Isotype switching (IgM to other Ig) of B-cells occurs in:

A

Germinal centers of lymphoid follicles on lymph node complex.

122
Q

Just remember this, it looks high yield

A

APC - B7 & MHC II ⇒ Antigen

Th - TCR & CD28

Activated Th - TCR & CD40L ⇒ Antigen

B-Cell - MHC II & CD40

– IL-4 = IgE // IL-5 = IgA –

123
Q

Heavy chain constant regions are _______ specific

A

isotype specific

(Tipos Heavy) - HEAVY = isoType specific.

124
Q

Light chains are _______ specific and do NOT determine isotype

A

light chain are antigen specific

125
Q

Cells that mediate Delayed-Type Hypersensitivity reactions (DTH)

(Contact dermatitis, granulomatous inflammation, tuberculin test, Candida extract skin reaction)

A

T-lymphocytes.

126
Q

Do Delayed-Type Hypersensitivity reactions (DHT) involve antibody or complement?

A

No.

127
Q

In DTH (Delayed-Type Hypersensitivity), antigen is taken up by __________ and presented to CD___+ lymphocytes on MHC class___ molecules.

A

dendritic cells (could be langerhans in skin!)

CD4+ lymphocytes (helper, usually Th1 lineage)

MHC class II molecules. (CD4+ = MHC II)

128
Q

When a tuberculin test is done, antigen is taken by dendritic cells and presented to CD4+ on MHC II, then activated Th1 lymphocytes secrete _______ which recruits ___________ leading to a monocytic infiltration on the site where antigen was introduced.

A

IFN - gamma activates macrophages.

129
Q

Predominant cells found on granulomas:

A
  • Epithelioid MACROPHAGES

- Multinucleated GIANT cells

130
Q

Every time there is a case where there is granuloma formation, you think about this process and cells interacting:

A

T cells ⇒ T helper kind (CD4+)

Think about MACROPHAGES and IL-12

Th1 cells = INF - gamma (Always in granuloma formation and if there are macrophages involved, think about IFN - gamma)

Activated macrophages = TNF - alpha (additional monocytes and macrophages to the area)

131
Q

What type of Th cell drives granuloma formation?

A

Th1

(Granulomas are bad because mycobacterium evade intracellular killing BUT control the infection because they PREVENT bacteria from SPREADING!)

132
Q

The right side of the body above diaphragm is drained by the ____ lymphatic duct into the junction of the right subclavian and internal jugular vein

A

Right

133
Q

The ______ ______ drains everything into junction of left subclavian and internal jugular veins

A

thoracic duct

134
Q

Rupture of thoracic duct can cause:

A

Chylothorax

135
Q

In splenic disfunction (splenectomy) there is:
__ IgM, ___ complement activation,

____ C3b opsonization and

____ suceptibility to encapsulated organisms

(> or <)

A

Less IgM <

Less complement activation <

Less C3b opsonization <

More suceptibility to encapsulated organisms >

136
Q

Vaccines that patients with splenectomy need:

A
  • Pneumococcal (Streptococcus pneumoniae)
  • Haemophilus influenzae type b (Hib)
  • Meningococcal (Neisseria meningitidis)
137
Q

Thymus is derived from:

A

Third pharyngeal pouch

138
Q

Thymoma (neoplasia of thymus) can be seen in:

A

Myasthenia gravis

Superior vena cava syndrome

139
Q

HLA subtype associated with myasthenia gravis and graves disease

A

B8 (BB-8)

140
Q

HLA associated with celiac disease

A

DQ2 / DQ8

(I ate (8) too (2) much gluten at Dairy Queen)

141
Q

HLA associated with Goodpasture syndrome, multiple sclerosis and hay fever

A

DR2

2 lungs, 2 kidneys, 2 doctors to treat goodpasture.

142
Q

HLA subtype associated with SLE

A

2,3 - SLE!

(DR2 and DR3)

143
Q

Rheumatoid arthritis is associated with HLA subtype:

A

DR4

144
Q

Main cell in charge of Delayed cell-mediated hypersensitivity (Type IV) and acute and chronic organ rejection

A

T cell

145
Q

T regulatory cells inhibit ___ cell function and express ______ and _______ in their surface

A

T regs inhibit Th1

Express CD25 and FoxP3 in their surface

146
Q

Autoimmune Polyendocrine Syndrome - 1 is due to:

A

AIRE deficiency - Omenn syndrome

(Autoimmune Regulator)

Protein is active primarily in the thymus (helping T cells distinguish the body’s own proteins from those of foreign invaders)

147
Q

Th1 cell activates macrophages and cytotoxic T cells (CD8+) to kill phagocytosed microbes by secreting:

A

IFN - gamma

148
Q

Genetic deficiency of FoxP3 in Tregs causes:

A

IPEX

  • Immune dysregulation
  • Polyendocrinopathy
  • Enteropathy
  • X-linked
149
Q

Diabetes in male infants + nail distrophy and dermatitis, you think of (Diabeto):

A

IPEX (FoxP3 deficiency on Tregs)

150
Q

Complement binding site and in which region is it located?

A

D.

Located in Fc region

(constant, carboxyl terminal, complement binding)

Determines isotype (IgG, IgD, etc)

151
Q

Mature, native B cells prior to activation express Ig__ and Ig__ on their surfaces

A

IgM and IgD

152
Q

MAC (Membrane Attack Complex) defends against gram ______ bacteria

A

Negative.

153
Q

Classic complement pathway invoves:

A

IgG or IgM

154
Q

Inhibitors of complement activation on self cells:

A

DAF (Decay Accelerating Factor) - CD55

and

Cl esterase inhibitor

155
Q

C1 esterase inhibitor deficiency causes:

A

Hereditary angioedema

(unregulated activation of kallikrein) and > bradykinin

(ACE inhibitors contraindicated)

156
Q

Prevention of formation of anchors for complement inhibitors such as DAF/CD55

A

Paroxysmal Nocturnal Hemoglobinuria

(complement-mediated lysis of RBCs)

157
Q

IFN - alpha and beta

  • Downregulate ______ _______ on virus infected cells
  • Upregulates _______ expression
A

Downregulate protein synthesis

Upregulates MHC expression

158
Q

EBV receptor on B cell

A

CD21

159
Q

Type of vaccine contraindicated in pregnancy and immunodeficiency (HIV < 200 cells)

A

- Live attenuated vaccines

(MMR, Adenovirus, Polio (sabin), Varicella, Smallpox, BCG,

Yellow fever, Influenza (intranasal), Rotavirus)

160
Q

Can toxoid cause disease?

A

No.

It’s only a denaatured bacterial toxin (only stimulates immune system but no infective potential)

161
Q

Serum sickness is a type ______ hypersensitivity reaction

A

III because it is an immune complex disease.

162
Q

Local subacute immune complex-mediated hypersensitivity reaction (Type III) that consists in:

  • Intradermal injection of antigen into a presensitized (IgG) individual that leads to immune complex formation in the skin

(Edema, necrosis and activation of complement)

A

Arthus reaction

163
Q

Contact dermatitis

Graft vs Host disease

PPD, patch test and candida extract

Are examples of:

A

Type IV hypersensitivity reactions

164
Q

T cell immune function can be tested with

A

Candida extract.

165
Q

Absent B cells in peripheral blood

Low Ig of all clases

Absent/scanty lymph nodes and tonsils

Live vaccines contraindicated

A

X-linked agammaglobulinemia (Bruton)

166
Q

Normal IgM and IgG levels

Low IgA

Susceptibility for Giardiasis

Most common primary immunodeficiency

A

Selective IgA deficiency

167
Q

Low plasma cells,

Low immunoglobulins

Presents AFTER age 2

Risk of autoimmune disease

A

Common variable immunodeficiency

168
Q

Child with disseminated mycobacterial and fungal infection AFTER administration of BCG vaccine

A

IL-12 receptor deficiency (low IFN - gamma)

169
Q

Impaired recruitment of neutrophils to site of infection +

  • Coarse facies
  • Staphylococcal cold abcess (noninflammed)
  • Retained primary teeth
  • High IgE
  • Eczema or dermatologic problems
  • Bone fractures from minor trauma
A

Autosomal dominant hyper IgE syndrome (Job)

170
Q

Deficiency of Th17 cells due to STAT3 mutation

A

AD Hyper IgE syndrome (Job)

171
Q

In a child who has absent cutaneous reaction to Candida antigens + presents noninvasive Candida albicans infections of skin and mucous membranes, they surely have:

A

T cell dysfunction

(Congenital genetic defects in IL-17 or receptor)

Chronic mucocutaneous candidiasis.

172
Q

Bone marrow transplant curative in this type of immunodeficiency

A

SCID (Severe Combined Immune Deficiency) B+T cells

173
Q

Cerebellar defects + spider angiomas + IgA deficiency

+ Higher risk for lymphoma and leukemia

A

Ataxia-telangiectasia

(Failure to halt progression of cell cycle + mutations accumulate)

174
Q

Defective CD40L on Th cells (CD4+)

A

Hyper IgM

175
Q

Falilure to make germinal centers

A
  1. SCID
  2. Hyper IgM

(Note: X-linked agammaglobulinemia NO because they just dont have MATURE B cells but they do show germinal centers - so only low circulating B cells.)

176
Q

Leukocytes and platelets unable to reorganize actin cytoskeleton

A

Wiskott-Aldrich

177
Q

Wiskott-Aldrich

A
  1. Thrombocytopenia
  2. Eczema
  3. Recurrent pyogenic infections
  4. high IgE and IgA
178
Q

Leukocyte adhesion deficiency clinical presentation:

A
  • ABSENT PUS
  • Delayed (more than 30 days) separation of umbilical cord
  • impaired wound healing
  • recurrent skin and mucosal BACTERIAL infections
  • MORE neutrophils in BLOOD but NOT in infection sites (can´t migrate)
179
Q

Defect in CD18 protein on phagocyte

A

Leukocyte adhesion deficiency

(impaired migration and chemotaxis)

“You can’t adhere until you’re eighteen, dear”

180
Q

Progressive neurodegeneration

Lymphohystiocytosis

Partial Albinism

Neuropathy

Recurrent pyogenic infections (Staph+strep)

Mild coagulation defects

A

Chediak Higashi syndrome

181
Q

Found this in child with Staph aureus infection. Dx?

A

Probably Chediak-Higashi

(Giant granules in granulocytes and platelets, pancytopenia)

182
Q

Why are cysteinyl-containing leukotrienes (LTC4, LTD4 and LTE4) important in asthma pathogenesis?

A

They cause bronchospasm and increase bronchial mucous secretion

183
Q

Lab technique that uses specific antibodies and a known quantity of radiolalbeled antigen to determine the amount of antigen present in an unknown sample

A

Radioimmunoessay

184
Q

In there is failure to bind antibody to specific radiolabeled antigen in a radioimmunoassay this indicates that:

A

When there is no binding after washing the plates, in a radioimmunoassay, it means that the available antibodies do not share epitopes with the antigen.

185
Q

If the radiolabeled and unlabeled antigens are identical (have the same epitopes), what happens in a radioinmunnoessay?

A

They should compete equally for antibody binding sites.

Increasing concentration of of antigen Y decreases measured radioactivity

186
Q

Erythroblastosis fetales or Fetal Disease of the Newborn is most commonly caused by:

A

Rhesus incompatibility (particularly the D antigen) (rh incompatibility)

187
Q

Findings in Rh+ fetus with Rh- mother

A
  • Release of immature, nucleated erythrocytes
  • extramedullary hematopoiesis (hepatosplenomegaly)
  • Anemia (autoimmune hemolysis)
  • Direct Coombs test +
  • Jaundice
  • Generalized edema (if hydrops fetalis)
188
Q

Which sensitization can occur during the first pregnancy?

a) ABO
b) Rh

A

ABO incompatibility can occur during first pregnancy but Ig in A and B is IgM (does NOT cross the placenta) so risk for Hemolitic Disease of the Newborn is minimal.

189
Q

What is one of the things that must happen before a fetus gets Hemolytic Disease of the Newborn due to Rh incompatibility?

A

The Rh- mother must have a previous Rh+ pregnancy

(because maternal immune system needs to have induced anti-Rh (D) IgG antibodies PRIOR to having a subsequent pregnancy)

190
Q

In which disease can we see nonimmune hydrops fetalis?

(negative coombs)

A

Fetuses with homocygous alpha-thalassemia (Barts) = severe functional anemia with coombs negative test.

191
Q

Which are the main cells implicated in Graft Vs Host Disease? (GVHD)

A
  • Donor surviving T cells from the graft
  • Recognized host MHC antigens as foreign
  • Donor CD4+ and CD8+ T cells = destruction
192
Q

Early signs of Graft Vs Host Disease (GVHD)?

A
  • Diffuse maculopapular rash (predilection for palms+soles and may desquamate)
  • GI tract involvement (diarrhea, intestinal bleeding, abominal pain)
  • Liver damage =abnormal liver function tests (except in liver transplant b/c liver T cells recognize liver as own = do not attack)
193
Q

Child with light skin and silvery hair + recurrent skin and respiratory infections + giant cytoplasmic granules in neutrophils and monocytes + neurologic abnormalities (paresthesias, nystagmus). Dx?

A

Chediak-Higashi

(AR disorder of neutrophil phagosome-lysosome fusion)

194
Q

Child with the next findings. Dx?

A

Wiskott - Aldrich syndrome

(WASP gene)

195
Q

Leukotriene B4 function

A

Chemotaxis

(most potent chemotactic eicosanoid)

196
Q

Is thromboxane A2 prothrombotic or antithrombotic?

A

Prothrombotic.

It induces vasoconstriction and platelet aggregation.

197
Q

Is prostacyclin prothrombotic or antithrombotic?

A

Antithrombotic.

Prostacyclin induces vasodilation and lessens platelet aggregation.

198
Q

Preceding infection in Reactive Arthritis

A
  • Genitourinary (Chlamydia trachomatis)
  • Enteritis (Salmonella, Shigella, Yersinia, Campylobacter, Clostridium difficile)
199
Q

Reactive Arthritis findings

(HLA-B27 b/c it’s a seronegative spondyloarthropathy)

A
  • Assymetric mono or oligoarthritis
  • Enthesitis
  • Dactylitis
  • Conjunctivitis/Anterior uveitis
  • Urethritis / Cervicitis / Prostatitis
  • Oral ulcers + ulcers hands or soles.
  • Sacroileitis may occur.
200
Q

When they ask about circulating maternal antibodies (Rh or ABO) always read and pay attention to number of child it is (second child in Rh? CAREFUL!)

A

This was a PSA.

201
Q

Cough, night sweats, weight loss and an upper lobe lesion on chest x-ray is:

A

Pulmonary TB

until proven otherwise.

202
Q

IL-12 function

A

Induces activated T helper cells to differentiate into Th1 cells.

203
Q

Finding:

A

Multinucleated Langhans cells

(predominant cells found in granulomas - TB)

204
Q

When a case tells you a patient has a Giardia lamblia infection, you immediately know his ______ levels are low or nonexistent.

A

IgA.

(most important Ig vs Giardia)

205
Q

If a patient CANNOT produce Immunoglobulins, which area of the lymph node is probably atrophic?

A

Germinal centers.

(B cells are in the Germinal centers. If there are no mature B cells, there are no Igs)

206
Q

Child with fever, dysphagia, drooling and a cherry red epiglottis with laryngoscopy probably has:

_____________ caused by_____________

A

Epiglottitis
caused by Haemophilus influenza type b in kids

Almost certainly caused by failed vaccination

207
Q

Toxic Shock Syndrome clinical presentation:

A
  • Fever, vomiting, diarrhea
  • Erythroderma (diffuse macular rash = sunburn)
  • Severe hypotension or multisystem failure
  • Elevated Transaminases, elevated CREATININE
  • Desquamation palms and soles
208
Q

Ethiology Toxic Shock Syndrome

A
  • Staphylococcus aureus producing:

Toxic Shock Syndrome Toxin (TSST)

SUPERANTIGEN that activates large number of T helper cells.

209
Q

Interleucins that cause capillary leakage, circulatory collapse, hypotension, shock, fever, skin findings and multiorgan failure in TSS secondary to TSST.

A

IL - 2 from T cells

IL - 1 and TNF from macrophages.

210
Q

Immunosupressive agent that inhibits lymphocyte proliferation by blocking IL-2 signal transduction

A

Sirolimus

(blocks mTOR that is necessary for IL-2 signal transduction)

211
Q

Proliferation signal inhibitor that targets mTOR (and thus, inhibits cell growth and proliferation)

Pathway that it inhibits

A

Sirolimus binds to FKBP and inhibits mTOR

Interrupts IL-2 signal transduction.

212
Q

Immunoinhibitory drug that selectively targets lymphocytes, reducing B and T cell proliferation and antibody production while promoting T cell apoptosis

A

Mycophenolate (inhibits de novo purine nucleotide synthesis - IMD inosine monophosphate dehydrogenase)

213
Q

Chimeric antibody directed against CD20 antigen

(specific to B lymphocytes)

A

Rituximab

214
Q

NK (Natural Killer Cells) are responsible for killing cells that:

A

have decreased of absent MHC class I protein on their surface.

215
Q

You encounter a cell that expresses CD16 or CD56 on its surface.

What type of cell is it?

With what can you activate it?

A

NK cell

Activated with IFN - gamma and IL-12

216
Q

AR deficiencies of the IFN - gamma receptor result in:

A

disseminated mycobacterial disease in early infancy or childhood (can happen with BCG vaccine stain)

217
Q

Defect in CD18 can predispose to:

A

Leukocyte adhesion deficiency

(delayed separation if umbilical cord, NO PUS, poor wound healing)

218
Q

Hep B serological marker that is detectable during acute infection and its persistence more than 6 months = chronic infection

A

HBsAg

219
Q

Hep B serological marker that indicates active viral replication and infectivity. (Detectable during acute infection)

a) HBsAg
b) HBeAg
c) Anti-HBc IgM
d) Anti-HBs
e) Anti-HBe
f) Anti-HBc IgG

A

b) HBeAg

“e” de es infeccioso

220
Q

First serological sign of Hep B infection

A

Anti-HBc IgM

(IgM de Mediato. Si HBc core es lo que te infecta de Hep B, entonces si ya tienen IgM contra HBc significa que tu cuerpo ya lo notó como infección “intruso”)

221
Q

Serological marker of Hep B that confers long-term immunity

Seen with:

  • Cleared infection
  • Vaccination
A

Anti-HBs

(Tiene a fuerza que ser anti algo. Cuando es “anti” el cuerpo ya reconoció al antígeno y trabajó para que ya no vuelva a infectar. Si HBs es lo que se ve en acute infection, Anti-HBs es lo que te va a proteger de desarrollar una acute infection)

222
Q

When the serologic of Hep B indicates presence of Anti-HBe, what does it mean?

A

Indicates less viral replication and infectivity, probably the person will be cured soon.

223
Q

If you find a patient with Anti-HBc IgG,
how would you think he acquired it?

A

In acute or chronic infection
Because Anti-HBc IgG is NOT present after vaccination.

224
Q

The presence of anti-HBc and anti-HBs antibodies in serum without detectable viral antigens indicates:

A

Recovery from acute hep B infection

225
Q

Patients with chronic hep B have elevated __________ levels ______ months after initial infection.

A

Chronic Hep B = elevated HBsAg >6 months after initial infection.

226
Q

Chronic Hep B with high infectivity presents with these levels:

A

Persistent elevation of:

  • HBsAg
  • HBeAg
  • HBV DNA

NO ANTI-HBeAg (indicates less viral replication and infectivity. They don’t have this)

227
Q

A patient vaccinated vs. Hep B has
a) Anti HBs antibodies

b) Anti HBeAg antibodies
c) Anti HBc antibodies

A

They have a) Anti HBs antibodies with NO Anti HBc nor Anti HBe
(because virus never directly infected them. They just got HBsAg from the vaccine and formed Anti HBsAg antibodies.

228
Q

Dendritic cells, macrophages and B-lymphocytes have in common that they present a _______ molecule

A

MHC class II molecule

Dendritic cells, macrophages and B-lymphocytes are all APCs

229
Q

MHC class II molecules are synthesized in __________

A

MHC class II molecules are synthetized in the Rough Endoplasmic Reticulum of APCs

230
Q 
After MHC class II molecules aggregate in the acidified phagolysosomes and degrade the invariant chain, they load antigen. 
MHC class II loads antigen and becomes a molecule-protein complex, they are displayed in the surface of APCs and are available to bind the \_\_\_\_\_\_\_ on \_\_\_\_\_\_\_\_\_\_ and initiate \_\_\_ cell response
A

MHC class II molecules bind the TCR on T-lymphocytes and initiate T cell response.

231
Q

Failure to acidify lysosomes leads to deficient expression of MHC __________ bound to foreign antigen and subsequent lack of interaction between ______ and ___ cells.

A

MHC class II

Lack of interaction between APCs and T cells.

232
Q

Sensitized Th2 cells in the airways promote isotype switching in B lymphocytes to IgE.

What substance do they produce to accomplish this switching?

A

Th2 –> IL - 4 —> IgE

233
Q

Sensitized Th2 cells also produce _____ which recruits eosinophils.

A

IL - 5

234
Q

Main difference between Th1 and Th2
CD4+ cells

Which one is for cell-mediated adaptive immunity + delayed-type hypersensitivity (IV)?

Which one for allergic response in type I hypersensitivity?

A

Th1 is for cell-mediated adaptive immunity (IC pathogens) and Type IV hypersens reactions (delayed)

Th2 contribute in type I hypersensitivity (allergic reactions + anaphylaxis)

235
Q

Which other IL apart from IL-4 do Th2 cells need to produce to promote B-cell immunoglobulin class switching to IgE ??

A

Th2 cells produce both:
IL-4 and IL-13
for class switch to IgE and mast cell priming

236
Q

Relate the columns:

A
  • *Th1** =
  • *IL-1:** fever and inflammation
  • *IL-3:** growth+differentiation bone marrow stem cells
  • *IFN-gamma:** Activates macrophages, stimulates CD8+ cells, inhibits Th2
  • *Th2** =
  • *IL-3**
  • *IL-5** = stimulates eosinophils
  • *IL-4 and IL-13** = promotes class switching IgE
237
Q

Findings in chronic lung transplant rejection:

A

MONTHS or YEARS after transplantation.

  • Progressive scarring of small airways (Bronchiolitis obliterans)
  • Obstructive lung disease (< FEV)
  • Dyspnea and dry cough
238
Q

If histology of a recent lung transplant receptor shows fibrinoid necrosis with hemorrhage and ischemia or “white graft” reaction, you typically think in __________ rejection

A

Hyperacute

239
Q

Most common microorganisms that can infect a person with Chronic Granulomatous Disease (NADPH oxidase deficiency)

A

Catalase POSITIVE + organisms destroy their own hydrogen peroxide (H2O2)

- Staphylococcus aureus

- Burkholderia cepacia

- Serratia marcescens

- Nocardia

- Aspergillus

240
Q

In tight adhesion and crawling, neutrophils become firmly attached to the endothelium by binding with ________ to ___________ on endothelial cells

A

CD 18 beta 2 integrins (Mac-1 and LFA-1)

to Intracellular Adhesion Mollecule (ICAM-1)

241
Q

Protein at the peripheral intercellular junction on endothelial cells that permits transmigration

A

PECAM-1
platelet endothelial cell adhesion molecule 1

242
Q

________ binds to Cyclophilin or FKBP to inhibit ______

A

Cyclosporine or Tacrolimus

bind to FKBP or cyclophilin

To inhibit Calcineurin

243
Q

Bcl - x and Bcl - 2 are ________ proteins

A

anti-apoptotic.

When there is a high level of Bcl-2, cells don’t die and errors accumulate.

244
Q

Caspases are _____________

A

proteolytic enzymes

cysteine-aspartic-acid-proteases

245
Q

Apoptosis can occur through either the intrinsic (mitochondia-mediated) pathway
or the extrinsic (receptor-initiated) pathway.

Both pathways converge in the activation of ________

A

Caspases.

246
Q

Clinical features of selective IgA deficiency

A
  • Recurrent sinopulmonary (pneumonia), gastrointestinal infections (Giardia)
  • Concommitant autoimmune disease (Celiac disease)
  • Anaphylaxis during blood transfusions
247
Q

When transfusing blood products (RBCs, platelets, fresh frozen plasma), IgA deficient patients may present:

A

Anaphylaxis.

IgA deficient patients should receive blood products that are washed of residual plasma
or from an IgA deficient-donor.

248
Q

Inactivated versions of the influenza vaccine (injection) function mainly by inducing ________ antibodies against the ___________ antigen

A

Neutralizing antibodies

against the Hemagluttinin antigen.

249
Q

For signs of inflammation to present in the injection of candida extract on the skin, we need these two cells:

A

CD4+ T cells and macrophages.

(These cells recruit CD8+ so in a way, they are also involved)

250
Q

Which of the following vaccines produces stronger immune responses by acting as a persistent stimulus to activate helper and cytotoxic T cells as well as by creating better IgA mucosal immunity?

a) Live-attenuated oral vaccine (Sabin)
b) Inactivated poliovirus (Salk) vaccine

A

Live attenuated oral vaccine (Sabin)

(intestinal exposure to novel antigens = mesenteric lymph nodes and peyer’s patches become activated and synthetize IgA = better mucosal immunity)

251
Q

After X-linked SCID, the second most common cause is:

A

Adenosine deaminase deficiency SCID

252
Q

In X-linked agammaglobulinemia flow cytometry, the main markers that would be low are:

  • CD4
  • CD8
  • CD15
  • CD16
  • CD19
A

CD19
Because Bruton agammaglobulinemia is failure of B cells to mature (and pre-B cells are CD19 and CD20 +) and panhypogammaglobulinemia (all Ig low)

253
Q

In this autoimmune disease, CD____ cells induce B cells to synthesize _________ ________ and
_______ __________ protein antibodies

A

CD4+ T cells

induce B cells to synthesize:
Rheumatoid Factor & Anti-Citrullinated protein antibodies (ACPAs)

254
Q

Rheumatoid factor is an antibody (IgM) specific for the _____ component or Ig___

A

Fc component of IgG

255
Q

People with CREST syndrome present _________ antibodies

A

CREST syndrome = Anticentromere antibodies

256
Q

People with SLE present this type of antibodies:

A
  • Anti-dsDNA antibodies
257
Q

The Monospot test assesses __________________
And it is positive in ________ __________ from ________ _____ Virus

A

serum’s ability to agglutinate sheep erythrocytes

Positive in infectious mononucleosis from

Epstein Barr Virus

258
Q

The _____ receptor is expressed on T-lymphocytes and plays an important role in DEATH and apoptosis. (Activation-induced cell death)

A

Fas

259
Q

People with SLE may have mutations involving ____ of _____ ligand resulting in excessive accumulation of autoreactive T cells and defect in activation-induced T lymphocyte death.

A

Fas or Fas ligand

260
Q

Individuals with IL-12 receptor deficiency suffer from severe mycobacterial infections (Th0 –>X –>Th1 )

Administration of _________ is indicated in this patients to activate macrophages.

A

IFN - gamma

261
Q

Th ——> Functions of IL-2

A
  • Stimulate growth of CD4+ and CD8+ cells and B cells
  • Activates NK cells
  • Activates Monocytes

01. Step 1 mine (4 decks)

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